Studies this year have centered on the pathophysiology of Leydig cell activation in patients with familial precocious puberty. This interesting group of patients with familial precocious puberty. This interesting group of patients demonstrate what appears to be gonadotropin independent Leydig cell activity. Previous studies have focussed on the possibility that a humoral factor is responsible for this process. Several groups have searched for this hypothetical factor using in vitro assays of Leydig cell function, usually the dispersed rat Leydig cell assay. These systems have failed to reveal Leydig cell stimulators. We reasoned that the heterologous nature to the assay systems might explain this failure. We examined this hypothesis by infusing plasma from patients with the disorder control group, and from pubertal stage matched controls directly into the spermatic artery of rhesus monkeys. Testosterone secretion into the testicular vein served as the response parameter. This system separated the precocious puberty group from the control group, supporting the hypothesis that a circulating factor may play a role is the pathogenesis of this syndrome.